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Free U.S. shipping on orders over $150TB500 peptide is a shorter, bioactive fragment of thymosin beta-4, designed to focus on thymosin beta-4’s most therapeutically relevant region, the 7-amino acid sequence LKKTETQ responsible for actin binding and tissue regeneration [1]. Though structurally simpler than the full-length thymosin beta-4, TB500 peptide retains potent biological activity [5]. The number 500 in TB500 is added as a commercial name, without biological or scientific significance.
Key biochemical features include:
TB500 exerts multi-system effects, supporting wound healing, reducing inflammation, promoting cell regeneration, and enhancing immune defenses [1].
TB500 accelerates tissue repair by binding actin, a key structural protein in cells. This interaction stimulates stem cell recruitment and differentiation at injury sites, migration of skin cells to close wounds faster, and formation of new blood vessels (angiogenesis) to improve oxygen and nutrient delivery [1].
It also enhances collagen alignment and increases laminin-5, both essential for strong and well-structured tissues [7]. Simultaneously, it reduces the number of scar-forming cells, minimizing fibrotic tissue formation [8].
Animal studies have confirmed TB500 peptide’s ability to reduce tissue damage, speed up recovery, and promote healing even in challenging conditions [9]. Human trials suggest that topical formulations are safe and effective in wound repair. Emerging data also support the potential role of TB500 in neurological and cardiac tissue regeneration, aiding recovery after events like stroke or heart attack [9].
Following tissue injury, high levels of inflammation can damage tissues and lead to permanent scarring. TB500 peptide mitigates this response, lowering the levels of inflammatory cells and the chemical signals they release [1]. This has downstream impacts of reducing tissue swelling, protecting healthy tissue, and creating an environment supportive of proper healing with less scar tissue formation [1].
A key anti-inflammatory mechanism involves the NF-kB signalling pathway, which controls the expression of many pro-inflammatory genes. TB500 inhibits NF-kB activation, prevents p65 subunit phosphorylation, and blocks nuclear translocation of NF-kB [10]. These actions have been demonstrated in corneal, cardiac, and liver tissues. The NF-kB inhibition contributes to reduced inflammation and improved healing responses in these tissues [10].
TB500 peptide modulates the toll-like receptor-4 (TLR-4) pathway, which is central to innate immune responses [11]. Through upregulation of microRNA-146a, TB500 can suppress this pathway, promoting anti-inflammatory effects [11]. For this reason, TB500 may indirectly support the repair of gut barriers by improving the proliferation and migration of cells, and supporting tissue healing processes.
Furthermore, a peptide fragment within TB500, Ac-SDKP, has been shown to reduce fibrosis (e.g., heart scarring after myocardial infarction), likely through similar anti-inflammatory and anti-proliferative mechanisms [6].
TB500 strengthens antimicrobial defenses by increasing the expression of antimicrobial peptides (AMPs) such as keratin 6A, CAMP, beta-defensins (BD2, BD3), and S100A8 [12]. These peptides help prevent bacterial adherence and enhance immune clearance of pathogens [12].
TB500 also boosts TLR4 expression, enhancing the recognition of bacterial invaders like LPS-producing pathogens [12]. When combined with antibiotics, TB500 enhances the activity of 12-LOX and 15-LOX enzymes, which promote resolution of inflammation and tissue restoration [12].
This synergy highlights TB500’s potential as an adjunct to antimicrobial therapies—supporting not only microbial defense but also repair of infected tissues.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Thymosin Beta-4 is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
What is Vesugen Peptide? Vesugen (also called vezugen) is a bioregulatory tripeptide with the amino sequence Lys-Glu-Asp [1], [2], developed based on the primary structure of polypeptides from animal organs. It was discovered at the Military Medical Academy in Russia alongside other anti-aging peptides like Epitalamin and Cortexin in Vladimir Khavinson’s group [3]. Vesugen Peptide Benefits, Mechanisms, and Side Effects Anti-Aging Benefits Vesugen may deliver vasoprotective and geroprotective benefits through epigenetic regulation of aging-related proteins, including: Decreasing Ki-67, a biomarker of aging. Ki-67 protein decreases during aging and in dissociated vascular endothelial cell cultures. Since vesugen physically interacts with the promoter region of the gene encoding Ki-67, vesugen may deliver vascular protective effects through epigenetic regulation of Ki-67 levels [4]. Increasing differentiation factors CXCL12 and WEGC1, which typically decline in aging cells. In fibroblast cell culture, vesugen increased these protein levels [5]. Increasing Sirtuin 1, which participates in DNA repair [6]. Increasing Growth-Associated Protein 43 (GAP43), which facilitates neurotransmission and neuroplasticity was increased after vesugen cell treatment [7]. Increasing Nestin, a protein marker of neuronal precursors, which was upregulated after vesugen cell treatment [7]. Side Effects A clinical studied treated 32 people aged 41-83 years with polymorbidity and organic brain syndrome in remission with vesugen. This treatment significantly slowed the rate of aging based on biological age indicators. Importantly, there were no changes in the degree of chromatin condensation, leading the authors to declare it safe on a nuclear genetic level [8]. Antioxidant and Cellular Protection Even though vesugen doesn’t have direct antioxidant activity, it can modify the structure of human lipoproteins and restrict lipid peroxidation [1]. On the other hand, a more recent study [8] performed on human subjects showed that Vesugen had pro-oxidant activity and the authors recommended against its use as an antioxidant. A 2008 study suggests that short regulatory peptides, including vesugen, decrease the percentage of dead cells in the neuronal population [1]. An important clinical trial done on 150 truck drivers affected by occupational factors demonstrated that administration of short bioregulating peptides which included vesugen restored psychoemotional status and enhanced stress resistance [9]. Moreover, in the mouse model of Alzheimer’s disease, a pronounced improvement in synaptic dendritic structures after administration of vesugen suggests that it may be able to restore neuroplasticity during early stages of Alzheimer’s disease [2]. Vascular and Sexual Health Atherosclerosis is a vascular disease characterized by lipid accumulation and plaque formation within arterial walls, resulting from endothelial injury associated with aging and oxidative stress. As arterial stiffening and narrowing from atherosclerotic plaque increase vascular resistance, hypertensive disorder may develop, which in turn further promotes endothelial damage and plaque progression [10]. Moreover, in vitro studies suggest that vesugen modulates endothelin-1 expression, potentially normalizing its levels and mitigating atherosclerotic and restenotic changes [6]. Vesugen was also investigated in 41 patients with vasculogenic erectile dysfunction as a manifestation of atherosclerosis. Clinical and instrumental parameters of blood flow in the main penile arteries before and after therapy showed that the blood flow through the main artery of the penis significantly improved [11]. Immunomodulatory effects Even though vesugen had no effect on differentiation capacity of immune cells of the pineal gland, it enhanced their proliferation potential [12]. In addition, Vesugen increased proliferative activity of thymocytes and activated their differentiation into regulatory T cells, preventing their apoptosis [7]. Since age-related reduction of thymus functional activity is an important cause of infections, vesugen could be of great benefit in boosting immunity.
What is Vilon? Vilon is a short synthetic dipeptide composed of lysine bound to glutamic acid (Lys-Glu). Vilon is considered a thymic peptide analogue, meaning it mimics biological activity associated with peptides produced by the thymus gland, an organ essential to immune system development. Like other bioregulatory peptides, Vilon has been studied for its ability to regulate protein synthesis and normalize cellular homeostasis, particularly in tissues affected by stress, aging, or immune dysfunction. While Vilon is not approved for medical use outside research settings, its small molecular structure enables high bioavailability and cell membrane permeability, characteristics that have made it an important subject in peptide-based therapy research. Vilon Peptide Benefits Immunomodulatory Vilon shows immunomodulatory properties, particularly its effects on thymus-dependent immune pathways. In an in vitro study using human monocytic THP-1 cells, Vilon treatment resulted in [1]: Increased cell proliferation activation via tyrosine phosphorylation of mitogen-activated kinases (MAPKs). Anti-inflammatory effects via suppression of tumor necrosis factor (TNF) and interleukin-6 (IL-6) even after exposure to LPS. A reduction in endothelial cell adhesion, a hallmark of decreased inflammatory activation. In Type 1 diabetes patients, administering Vilon resulted in [2]: Improved coagulation parameters by increasing antithrombin III and protein C, while also stimulating fibrinolysis. Reduced the required insulin dosage to maintain stable glucose metabolism. Reduced elevated T-helper cells and natural killer (NK) cell subpopulations. Restored levels of active T-lymphocytes, B-lymphocytes, and immunoglobulin A (IgA). Increased baseline insulin production and thereby decreased insulin need by 9 units. Anti-aging and regenerative Vilon has been investigated within the field of bioregulatory peptide research for its potential role in cellular repair, longevity regulation, and tissue regeneration. A case series examined 250 adults aged 65–87 with chronic periodontitis along with type II diabetes, atherosclerosis, and other cardiovascular diseases. Subjects received 10–20 µg daily submucosally for 5–10 days. The treatment significantly improved immune, oxidative stress, and coagulation parameters. Vilon treatment also reduced periodontal pocket depths by 1.2 Ramfjord index points and papillary marginal alveolar index by 10 times. These benefits, however, happened to a lesser degree in younger people with chronic periodontitis [3]. Age-associated declines in phosphorylated CREB (pCREB) reduce levels of arylalkylamine N-acetyltransferase (AANAT), contributing to age-related declines in melatonin, circadian rhythm, and sleep disruption. Rat pinealocytes were treated with either control (no treatment), norepinephrine (NE) 1 µg/ml (positive control), or peptide-treated cultures (epithalone or Vilon) at 100 ng/ml. Subsequently, cultures were incubated for up to 3 hours at 36.7°C in 5% CO2 [4]. Results showed that Vilon: Induced a 7-fold rise in pCREB expression after 1 hour. However, the effect was transient, returning to control levels within 2–3 hours. Produced a short-term stimulation of AANAT expression at 1 hour, but this effect diminished with prolonged exposure. Vilon peptide transiently enhances early transcriptional activation (pCREB) and enzyme induction (AANAT) in pinealocytes, suggesting it plays a regulatory role in stimulating melatonin synthesis at the initial phase of the signaling cascade. Aging is often associated with increased chromatin condensation (heterochromatinization), which suppresses gene expression. Another cell study investigated the effects of Vilon on chromatin organization in cultured lymphocytes obtained from elderly individuals [5]. The results demonstrated that Vilon loosened chromatin both globally and in the nucleolus, restoring access to genes silenced during aging. Apoptosis modulation and anti-cancer Vilon plays an apoptoregulatory role, helping to protect somewhat damaged healthy cells. However, in cancer cells, Vilon seems to increase apoptotic cell death, which can help prevent further cancer progression. In a cell study, administration of Vilon administered to rat spleen lymphocytes post-radiation induced significantly less apoptosis [6]. To date, the exact mechanisms by which apoptosis is inhibited has not been elucidated. In rats transplanted with carcinoma, Vilon stimulated apoptosis in both young and old rats, suggesting that instead of protecting damaged cells, Vilon plays a more apoptoregulatory role [7]. Because dysregulated apoptosis is a hallmark feature of carcinogenesis, some studies have explored Vilon’s effects in oncological research settings. Early experimental reports from Russian investigators suggest that Vilon could serve as an adjuvant to cancer therapy, resulting in [8]: Increased 2-year survival of patients Prevention of post-operative complications Reduced recurrences and tumor dissemination However, such studies remain experimental, and no clinical evidence currently supports Vilon for use in oncology. Vilon’s role in apoptoregulation continues to be a subject of research in the broader field of cellular homeostasis and peptide-based cytoprotection.
